1. Description of the problem

Arrhythmias: Up to one third of cardiothoracic surgery patients develop supraventricular tachycardias postoperatively. More malignant ventricular arrhythmias are much less frequent (approximately 2%), but are potentially fatal.

Bleeding: There are many factors that predispose patients to bleeding in the immediate postoperative period. It is important to identify the cause(s) of coagulopathy- particularly surgical bleeding- and treat the patient accordingly.

Acute Kidney Injury: AKI develops in 30-40% of cardiothoracic patients postoperatively. There is variability in the severity of renal dysfunction, but even a mild renal injury portends increased postoperative morbidity and mortality.

Low Cardiac Output: Ensuring maintanence of an adequate cardiac output is a cornerstone of management of the postoperative cardiothoracic surgery patient. Cardiac Index, which is expressed as liters per square meter, is the customary clinical measure of cardiac performance.

2. Emergency Management

Arrhythmia

Atrial and ventricular arrhythmias should be managed as per AHA/ACC Advanced Cardiac Life Support (ACLS) Guidelines.

Urgent cardioversion of any arrhythmia is indicated if it leads to:

-Chest pain

-Shortness of breath

-Hypotension

-Altered mental status

or in the presence of ventricular fibrillation or pulseless ventricular tachycardia.

Bleeding

Urgent re-exploration is indicated if:

-There is indication of cardiac tamponade

-The patient is hemodynamically unstable secondary to hypovolemia

Distinguish surgical bleeding from a postoperative coagulopathy.

Establish the rate of bleeding per 15 minutes.

Determine and monitor the hemodynamic status of the patient.

Acute Kidney Injury

Once renal dysfunction becomes evident, prompt and aggressive strategies are required to prevent irreversible dysfunction or the need for dialysis.

Cardiac function should be optimized; a higher target mean arterial pressure (80-100 mmHg) may be required in some chronically hypertensive patients.

Careful fluid challenges are given to increase preload, as required.

Inotropic support can be used to improve cardiac contractility.

All potentially nephrotoxic drugs (particularly ACEi/ARBs or NSAIDs) should be stopped.

Thromboelastogram - can give a rapid overview of clotting derangements.

A comparison of the blood hematocrit between a freshly drawn sample and one from the chest tube will differentiate lymphatic drainage or excessive serum reflux from fresh bleeding.

Acute Kidney Injury

The RIFLE and Acute Kidney Injury Network (AKIN) criteria have been established to define AKI within any setting and have been widely adopted within intensive care medicine.

RIFLE is an acronym for Risk (R), Injury (I), Failure (F), Loss (L) and End stage (E) based on increases in serum creatinine or oliguria.

R, I and F are defined as increases in serum creatinine of 50%, 100% or 200% or oliguria for 6, 12 or 24 hours, respectively.

Loss is defined as AKI persisting >4 weeks.

End stage is defined as >3 months.

The AKIN working group has defined AKI as a reduction in kidney function over a period of 48 hours.

This is manifest as an absolute increase in serum creatinine of 0.3 mg/dl (25 μmol/L), or a relative increase in creatinine of 50% or more.

A documented oliguria of <0.5 mL/Kg/hr for >6 hours despite adequate fluid resuscitation is also considered AKI.

The AKIN group advocates 3 stages of AKI based on the R, I and F categories of RIFLE, where stage 1 is defined using the same criteria as R, and stages 2 and 3 are I and F respectively.

There is also increasing evidence to support the use of novel urinary and serum biomarkers (such as neutrophil gelatinase-associated lipocalin kidney injury molecule-1, and cystatin C) to improve the early and accurate diagnosis of AKI in the setting of intensive care.

Though the evidence supporting the use of these markers is growing, they are not yet in widespread use.

Low Cardiac Output

A normal cardiac index (CI) after surgery is between 2 and 4.4 L/min/m2.

Arteriovenous difference is calculated by (SaO2 - SvO2) x 1.39(Hb) x 10, where SaO2 is the arterial saturation and SvO2 is the venous saturation.

CI is calculated by dividing CO by body surface area.

In the absence of available CO measurements, the CI will usually be >2.5 L/min/m2 if MAP 70-80 mmHg, urine output > 1 ml/kg/hr, base deficit < 2, skin temperature 36.5 -37.5 degrees and there are palpable pedal pulses.

To further delineate the cause of the low cardiac output, the following investigations should be considered:

Chest x-ray can rule out the presence of a pneumothorax.

ECG to exclude any new ST-segment changes indicative of potential new coronary artery or conduit occlusion.

Complete blood count to assess any drops in Hb or hematocrit indicative of ongoing bleeding, as well as leukocyte count elevation from underlying sepsis.

Echocardiography (preferably transesophageal) is most useful and will aid in the diagnosis of cardiac tamponade, new valvular dysfunction, regional wall motion abnormalities suggesting underlying ischemia, as well as right ventricular dysfunction.

Labortatory investigations for bleeding:

Complete blood count

Coagulation profile including INR and aPTT

Activated clotting time (ACT) is usually done at in the ICU.

Fibrinogen

Calcium

Thromboelastogram

4. Specific Treatment

Arrhythmia

Arrhythmias should be managed as per AHA/ACC Advanced Cardiac Life Support (ACLS) guidelines.

Prophylactic use of beta-blockers has decreased the incidence of atrial fibrillation by 70-80%.

In postoperative patients with atrial fibrillation, ensure that electrolytes are replete and there is no underlying sepsis.

Beta-blockers are first line for ventricular rate control, and amiodarone can be used to attempt chemical cardioversion.

Vernakalant is a novel, relatively atrial selective, anti-arrhythmic drug that has shown efficacy in the cardioversion of atrial fibrillation to sinus rhythm in a post-CABG cohort.

Contraindications to the use of an IABP include severe atherosclerosis of the iliofemoral vessels, aortic dissection and aortic insufficiency.

The optimal timing of placement for IABPs remains controversial, including which high-risk group may benefit from prophylactic placement.

5. Disease monitoring, follow-up and disposition

Patients with persistent atrial fibrillation postoperatively should be started on anticoagulation to decrease the risk of CVA. Elective DC cardioversion can be carried out 6-8 weeks after discharge if the patient remains in atrial fibrillation at this time.

If bleeding is due to a coagulopathy, there should be a resolution of bleeding once the coagulopathy has been reversed. If the patient continues to bleed with a normal temperature and coagulation profile, the cause of the bleeding is likely to be surgical in nature.

Ensure chest drains do not clot off, giving the false impression of resolution of the bleeding.

If CO is not improving with the addition of inotropes, an urgent echocardiogram should be obtained and cardiology consultation should be considered.

The possible etiology of the reduced function should be defined (see pathophysiology section below).

Follow-up with a nephrologist is advised for patients who have developed postoperative AKI, whether the serum creatinine returns to baseline postoperatively or not.

Pathophysiology

Arrhythmia

The mechanism for postoperative atrial fibrillation is not well understood, but it is thought to include multiple wavelet reentry in the atria, rapid firing of an atrial focus, or rarely atrial ischemia.

Ventricular tachycardia following CABG is often related to areas of scarring from underlying ischemia.

The scarring in the LV forms a substrate for reentry.

Patients with a history of larger infarcts and as a result poorer LV function are more likely to develop VT.

Bleeding

Medical bleeding may be due to:

--An elevated activated clotting time (ACT). This may be due to the administration of heparin during surgery or "pump blood" in the ICU.

--Preoperative treatment with platelet inhibitors such as aspirin, clopidogrel, and prasugrel

These effects are related to the effects on renal physiology of the sustained period of hyopthermic, nonpulsatile low-flow renal perfusion associated with bypass, as well as the endocrine and CNS effects of major surgery.

Vasoconstriction occurs secondary to angiotensin II and an increase in catecholamines.

Activation of the renin-angiotensin-aldosterone system promotes sodium and water retention and potassium excretion

Complement, bradykinin and kallikrein are increased, increasing capillary permeability and causing a fluid shift into the interstitium.

Low Cardiac Output

The etiologies of low cardiac output can be subdivided into pre-, intra- and post-operative causes.